A simple mathematical model of spontaneous electrical activity in a single smooth muscle cell.
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Biomedical subjects
Publications and source records attributed to M E Holman.
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1. Excitatory junction potentials (e.j.p.s) were recorded from smooth muscle cells of the saphenous arteries of young rabbits. 2. The amplitudes of e.j.p.s recorded from different preparations, in response to a single maximal stimulus, were small and variable (5--14 mV). They decayed exponentially with a time constant of about 200 msec. 3. At frequencies greater than 1 Hz the shape of those e.j.p.s which exceeded 12--15 mV in amplitude was changed. The early part of the e.j.p.s became faster in time course. 4. Trains of up to five stimuli, at frequencies greater than 4 Hz, caused summation of e.j.p.s; 'active responses' were superimposed on this depolarization. Peak amplitude of the response to repetitive stimulation was 50 mV. 5. In normal solution, contraction appeared to be associated with a change in the configuration of e.j.p.s. 6. No action potentials resembling those recorded from most visceral smooth muscles were observed in normal solutions although these could be evoked in the presence of TEA (2.5--10 mM). 7. The method of Abe & Tomita (1968) was used to determine the values of the length constant (lambda) and time constant (tau) of the smooth muscle of intact arteries. The value of lambda (0.6 mm) was about half that found for circular strips cut from larger arteries. 8. The time constant of decay of single e.j.p.s of less than 12 mV in amplitude was indistinguishable from the membrane time constant. 9. Noradrenaline caused contraction of the artery in the absence of a change in membrane potential. 10. It is tentatively suggested that there may be two different populations of receptors in this smooth muscle membrane.
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1. Contractions of the mouse vas deferens in response to electrical stimulation differ form those recorded form the guinea-pig vas deferens in that they are abolished by tetrodotoxin. 2. Changes in membrane potentials were recorded form the smooth muscle of both preparations in response to stimulation with current pulses applied by an intracellular electrode and by alrge extracellular plate electrodes. 3. Both preparations behaved similarly in response to intracellular stimulation. Electrotonic potentials in response to extracellular current pulses spread in a longitudinal direction in the guinea-pig vas deferens in accordance with the cable-like properties of this preparation. In contrast, no longitudinal spread of eletrotonus was observed in the mouse vas deferens. 4. Responses to nerve stimulation differed in the two preparations. In the guinea-pig, single stimuli caused excitatory junction potentials (e.j.p.s) which gave rise to action potentials. Some cells from the mouse vas deferens showed similar e.j.p.s and action potentials, although the threshold for the initiation of action potentials was lower and more variable. 5. The majority of cells in the mouse vas deferens failed to show action potentials in response to a single stimuli even though the amplitude of e.j.p.s was from 35 to 40 mV. This was probably due to the large resting membrane potentials of these cells, as all-or-nothing action potentials could be evoked if successive e.j.p.s were allowed to sum with each other or if a depolarizing current pulse was applied at the peak of an e.j.p. 6. The nature of the response to nerve stimulation recorded from differnt cells in the mouse vas deferens could be correlated with the amplitude and time course of the response of the same cell to intracellular stimulation. 7. It is concluded that individual smooth muscle cells in both preparations are probably coupled electrically but that there are few, if any, low resistance pathways in the longitudinal direction in the mouse vas deferens.
The distribution of vesicles in axon varicosities was examined in rabbit jejunum and opossum esophagus. Circular muscle cells of both rabbit jejunum and opossum esophagus responded to stimulation of intrinsic nerves with inhibitory junction potential in nearly all cases. Inhibitory junction potentials were rare and small in longitudinal muscle cells of rabbit jejunum. There were few axon varicosities with a predominance of large opaque vesicles or large dense-cored vesicle in any muscle layer of rabbit or opossum or in the plexuses of rabbit jejunum. There were almost as high a proportion of such varicosities in longitudinal as in circular muscle of rabbit jejunum, and there were almost none in circular muscle of opossum esophagus. The distribution of vesicles in varicosities was found often to be heterogeneous and could account for the observed occurrence of a small proportion of varicosities with a predominance of large vesicles. It is suggested that there is no structural distinction in vertebrates between axons which are cholinergic and axons which are nonadrenergic inhibitory.
The membrane potential of smooth muscle cells in the circular layer of the guinea pig ileum was recorded using intracellular electrodes. Transmural stimulation, in the presence of atropine, caused a transient hyperpolarization, an inhibitory junction potential (IJP). IJP's are thought to result from the action of transmitter released from intramural inhibitory nerves. It has been reported that, in the guinea pig jejunum, the amplitude of the IJP resulting from field stimulation is not altered by changes in the calcium and magnesium ion concentration in the bathing solution. Experiments reported here have shown that the IJP amplitude decreased markedly on reducing the calcium ion concentration and or increasing the magnesium ion concentration. Indirect evidence is presented suggesting that the decrease in amplitude of the IJP is due to a decrease in the amount of transmitter released.
1. Intracellular recordings were made from myenteric neurones of the guinea-pig small intestine in preparations which had a synaptic input from an orally situated segment of intestine. 2. Excitatory synaptic potentials could be evoked in most neurones by distension of the attached intestinal segment. 3. It was possible to distinguish two distinct firing patterns of synaptic potentials in response to distension. A transient short latency discharge was recorded from some neurones. From the others, a persistent synaptic discharge was recorded only after a long latency (2-11 sec). 4. Distension of intestinal segments evoked short latency transient inhibitory junction potentials in the circular muscle layer followed by excitatory junction potentials in both the circular and longitudinal muscle layers. 5. It is suggested that distension may cause both descending inhibition and, after a delay, descending excitation of the guinea-pig small intestine.